Atrial fibrillation is an irregular, rapid, chaotic heart rhythm disorder that is a chronic and debilitating medical condition. It is the most common cardiac arrhythmia and accounts for one-third of all hospitalizations for cardiac rhythm disorders in the United States. Patients with atrial fibrillation experience increased morbidity including lower exercise tolerance, frequent palpitations and heart failure. Atrial fibrillation is particularly prevalent in patients with heart failure and patients with both diseases are at risk for increased mortality. In particular, left ventricular hypertrophy and diastolic dysfunction are independent risk factors for the development of atrial fibrillation and both are associated with a higher incidence of atrial fibrillation. Antiarrhythmic drug therapy for atrial fibrillation is relatively ineffective for restoring and maintaining sinus rhythm and is associated with multiple side effects. The discovery that ectopic foci arising from the pulmonary veins trigger atrial fibrillation has led to catheter-based pulmonary vein isolation as an effective therapy for atrial fibrillation. Pulmonary vein isolation offers benefits over antiarrhythmic drugs but present techniques are associated with procedural risks and are less efficient in patients with left ventricular hypertrophy.
In the setting of abnormal ventricular function, atrial structural changes such as dilatation and fibrosis are prevalent and promote arrhythmogenesis. Normalization of ventricular function, by inhibiting angiotensin, appears to partially reverse atrial structural changes and reduce atrial arrhythmogenesis. Experimental and clinical evidence support the ability of angiotensin-inhibition to reduce atrial fibrillation, however evidence also exists that angiotensin-independent pathways contribute to atrial structural remodeling and atrial fibrillation.